Increasing Awareness of and Concern About Contrast-induced Nephropathy

Login or register to view PDF.
US Cardiology 2006;2005:2(1):140-144


The use of iodinated contrast media (CM) for both diagnostic imaging and interventional studies continues to increase. The introduction of multi-detector computed tomography (MDCT) scanners allows for quicker imaging of internal organs, and image acquisition is now fast enough for study of the coronary arteries. This technology requires the delivery of a high concentration of iodine to the vascular system and precise timing of the image acquisition.

With this expansion of the use of iodinated CM, the nature of the patients is also changing. More patients with chronic conditions, such as atherosclerotic cardiovascular disease, renal insufficiency, and congestive heart failure, are becoming candidates for contrast studies. Patients in emergency rooms with trauma, respiratory symptoms, and acute sepsis syndrome are also being sent for contrast-enhanced imaging. The consequence of the technological improvements and increased burden of disease in patients is that more patients are at risk for the development of contrast-induced nephropathy (CIN).

CIN remains defined by changes in serum creatinine. An increase of 25%, or more than 0.5mg/dL over baseline levels, is recognized as a significant change in renal function and is predictive of both in-hospital and out-of-hospital adverse events. However, creatinine is a relatively inaccurate marker of glomerular filtration rate (GFR) and, thus, renal function, because it is excreted in the urine as a result of both filtration and secretion. Furthermore, when GFR changes acutelyÔÇöfollowing a toxic insult, for exampleÔÇöcreatinine rises slowly, usually over days.Thus, there is a delay in the recognition of renal injury when using the serum creatinine. Other markers of GFR, such as cystatin C, appear to be more sensitive and accurate but have not found widespread application in clinical medicine.

Pathogenesis of CIN and Risk Factors

The pathogenesis of CIN remains complex and involves both toxic and ischemic injury to the kidney. The toxic effect, evident in vitro, is mediated at least in part by the generation of free oxygen radicals. These reactive oxygen species produce injury to the renal tubular cells and lead the cells towards apoptosis. The situation is exacerbated, particularly in the medulla of the kidney, by a reduction in medullary blood flow and oxygen delivery caused by CM. The nephron segments within the medulla include the loop of Henle; this part of the nephron has the highest oxygen consumption because of the active transport of sodium out of the urine. A reduction in medullary blood flow therefore creates critical hypoxia, causing cell necrosis.